Rapid eye movement sleep

From Infogalactic: the planetary knowledge core
(Redirected from REM sleep)
Jump to: navigation, search
EEG of a mouse. REM sleep is characterized by prominent theta-rhythm

Rapid eye movement sleep (REM sleep, REMS) is a unique phase of mammalian sleep characterized by random movement of the eyes, low muscle tone throughout the body, and the propensity of the sleeper to dream vividly. This phase is also known as paradoxical sleep (PS) and sometimes desynchronized sleep because of physiological similarities to waking states, including rapid, low-voltage desynchronized brain waves. Electrical and chemical activity regulating this phase seems to originate in the brain stem and is characterized most notably by an abundance of the neurotransmitter acetylcholine, combined with a nearly complete absence of monoamine neurotransmitters histamine, serotonin, and norepinepherine.[1] The cortical and thalamic neurons of the waking or paradoxically sleeping brain are more depolarized—i.e., can "fire" more readily—than in the deeply sleeping brain.[2] The right and left hemispheres of the brain are more coherent in REM sleep, especially during lucid dreams.[3]

REM sleep is punctuated and immediately preceded by PGO (ponto-geniculo-occipital waves) waves, bursts of electrical activity originating in the brain stem.[4] These waves occur in clusters about every 6 seconds for 1–2 minutes during the transition from deep to paradoxical sleep.[5] They exhibit their highest amplitude upon moving into the visual cortex and are a cause of the "rapid eye movements" in paradoxical sleep.[6][7]

Brain energy use in REM sleep, as measured by oxygen and glucose metabolism, equals or exceeds energy use in waking. The rate in non-REM sleep is 11–40% lower.[8]

Chemicals in brain

Compared to slow-wave sleep, both waking and paradoxical sleep involve higher use of the neurotransmitter acetylcholine, which may cause the faster brainwaves. The monoamine neurotransmitters norepinephrine, serotonin and histamine are completely unavailable. Injections of acetylcholinesterase inhibitor, which effectively increases available acetylcholine, have been found to induce paradoxical sleep in humans and other animals already in slow-wave sleep. Carbachol, which mimics the effect of acetylcholine on neurons, has a similar influence. In waking humans, the same injections produce paradoxical sleep only if the monamine neurotransmitters have already been depleted.[9][10][11][12][13]

Two other neurotransmitters, orexin and gamma-Aminobutyric acid (GABA), seem to promote wakefulness, diminish during deep sleep, and inhibit paradoxical sleep.[9][14]

Unlike the abrupt transitions in electrical patterns, the chemical changes in the brain show continuous periodic oscillation.[15]

Role of brain stem

Neural activity during REM sleep seems to originate in the brain stem, especially the pontine tegmentum and locus coeruleus. According to the activation-synthesis hypothesis proposed by Robert McCarley and Allan Hobson in 1975–1977, control over REM sleep involves pathways of "REM-on" and "REM-off" neurons in the brain stem. REM-on neurons are primarily cholinergic (i.e., involve acetylcholine); REM-off neurons activate serotonin and noradrenaline, which among other functions suppress the REM-on neurons. McCarley and Hobson suggested that the REM-on neurons actually stimulate REM-off neurons, thereby serving as the mechanism for the cycling between REM and non-REM sleep.[9][10][12][16] They used Lotka–Volterra equations to describe this cyclical inverse relationship.[17] Kayuza Sakai and Michel Jouvet advanced a similar model in 1981.[14] Whereas acetylcholine manifests in the cortex equally during wakefulness and REM, it appears in higher concentrations in the brain stem during REM.[18] The withdrawal of orexin and GABA may cause the absence of the other excitatory neurotransmitters.[19]

Research in the 1990s using positron emission tomography confirmed the role of the brain stem. It also suggested that, within the forebrain, the limbic and paralimbic systems, generally connected with emotion showed more activation than other areas. The areas activated during REM sleep are approximately inverse to those activated during non-REM sleep.[8]

Eye movements

Most of the eye movements in “rapid eye movement” sleep are in fact less rapid than those normally exhibited by waking humans. They are also shorter in duration and more likely to loop back to their starting point. About seven of such loops take place over one minute of REM sleep. Whereas in slow-wave sleep the eyes can drift apart, the eyes of the paradoxical sleeper move in tandem.[20] These eye movements follow the ponto-geniculo-occipital waves originating in the brain stem.[6][7] The eye movements themselves may relate to the sense of vision experienced in the dream, but a direct relationship remains to be clearly established. It does happen that congenitally blind people, who do not typically have visual imagery in their dreams, still move their eyes in REM sleep.[8]

Circulation, respiration, and thermoregulation

Generally speaking, the body suspends homeostasis during paradoxical sleep. Heart rate, cardiac pressure, cardiac output, arterial pressure, and breathing rate quickly become irregular when the body moves into REM sleep.[21] In general, respiratory reflexes such as response to hypoxia diminish. Overall, the brain exerts less control over breathing; electrical stimulation of respiration-linked brain areas does not influence the lungs, as it does during non-REM sleep and in waking.[22] The fluctuations of heart rate and arterial pressure tend to coincide with PGO waves and rapid eye movements, twitches, or sudden changes in breathing.[23]

Erections of the penis (nocturnal penile tumescence or NPT) normally accompany REM sleep in rats and humans.[24] If a male has erectile dysfunction (ED) while awake, but has NPT episodes during REM, it would suggest that the ED is from a psychological rather than a physiological cause. In females, erection of the clitoris (nocturnal clitoral tumescence or NCT) causes enlargement, with accompanying vaginal blood flow and transudation (i.e. lubrication). During a normal night of sleep the penis and clitoris may be erect for a total time of from one hour to as long as three and a half hours during REM.[25]

Body temperature is not well regulated during REM sleep, and thus organisms become more sensitive to temperatures outside their thermoneutral zone. Cats and other small furry mammals will shiver and breathe faster to regulate temperature during NREMS but not during REMS.[26] With the loss of muscle tone, animals lose the ability to regulate temperature through body movement. (However, even cats with pontine lesions preventing muscle atonia during REM did not regulate their temperature by shivering.)[27] Neurons which typically activate in response to cold temperatures—triggers for neural thermoregulation—simply do not fire during REM sleep, as they do in NREM sleep and waking.[28]

Consequently, hot or cold environmental temperatures can reduce the proportion of REM sleep, as well as amount of total sleep.[29][30] In other words, if at the end of a phase of deep sleep, the organism's thermal indicators fall outside of a certain range, it will not enter paradoxical sleep lest deregulation allow temperature to drift further from the desirable value.[31] This mechanism can be 'fooled' by artificially warming the brain.[32]


REM atonia, an almost complete paralysis of the body, is accomplished through the inhibition of motor neurons. When the body shifts into REM sleep, motor neurons throughout the body undergo a process called hyperpolarization: their already-negative membrane potential decreases by another 2–10 millivolts, thereby raising the threshold which a stimulus must overcome to excite them. Muscle inhibition may result from unavailability of monoamine neurotransmitters, the abundance of acetylcholine in the brainstem, and perhaps from mechanisms used in waking muscle inhibition.[33] The medulla oblongata, located between pons and spine, seems to have the capacity for organism-wide muscle inhibition.[34] Some localized twitching and reflexes can still occur.[35]

Lack of REM atonia causes REM behavior disorder, sufferers of which physically act out their dreams.[36] (An alternative explanation of this relationship is that the sleeper "dreams out the act": that the muscle impulse precedes the mental image. This explanation could also apply to normal sleepers whose commands to their muscles are suppressed.)[37] (Note that conventional sleepwalking takes place during slow-wave sleep.)[38] Narcolepsy by contrast seems to involve excessive and unwanted REM atonia—i.e., cataplexy and excessive daytime sleepiness while awake, hypnagogic hallucinations before entering slow-wave sleep, or sleep paralysis while waking.[39] Other psychiatric disorders including depression have been linked to disproportionate REM sleep.[40] Patients with suspected sleep disorders are typically evaluated by polysomnogram.[41][42]

Lesions of the pons to prevent atonia have induced functional “REM behavior disorder” in animals.[43]



Rapid eye movement sleep has since its discovery been closely associated with dreaming. Waking up sleepers during a REM phase is a common experimental method for obtaining dream reports; 80% of neurotypical people can give some kind of dream report under these circumstances.[44] Sleepers awakened from REM tend to give longer more narrative descriptions of the dreams they were experiencing, and to estimate the duration of their dreams as longer.[8][45] Lucid dreams are reported far more often in REM sleep.[46] (In fact these could be considered a hybrid state combining essential elements of REM sleep and waking consciousness.)[8] The mental events which occur during REM most commonly have dream hallmarks including narrative structure, convincingness (experiential resemblance to waking life), and incorporation of instinctual themes.[8]

Hobson and McCarley proposed that the PGO waves characteristic of “phasic” REM might supply the visual cortex and forebrain with electrical excitement which amplifies the hallucinatory aspects of dreaming.[11][16] However, people woken up during sleep do not report significantly more bizarre dreams during phasic REMS, compared to tonic REMS.[45] Another possible relationship between the two phenomena could be that the higher threshold for sensory interruption during REM sleep allows the brain to travel further along unrealistic and peculiar trains of thought.[45]

Some dreaming can take place during non-REM sleep. “Light sleepers” can experience dreaming during stage 2 non-REM sleep, whereas “deep sleepers”, upon awakening in the same stage, are more likely to report “thinking” but not “dreaming”. Certain scientific efforts to assess the uniquely bizarre nature of dreams experienced while asleep were forced to conclude that waking thought could be just as bizarre, especially in conditions of sensory deprivation.[45][47] Because of non-REM dreaming, some sleep researchers have strenuously contested the importance of connecting dreaming to the REM sleep phase. The prospect that well-known neurological aspects of REM do not themselves cause dreaming suggests the need to re-examine the neurobiology of dreaming per se.[48] Some of the old guard in paradoxical sleep research (Dement, Hobson, Jouvet), however, tend to resist the idea of disconnecting dreaming from REM sleep.[8][49]


After waking from REM sleep, the mind seems “hyperassociative”—more receptive to semantic priming effects. People awakened from REM have performed better on tasks like anagrams and creative problem solving.[50]

Sleep aids the process by which creativity forms associative elements into new combinations that are useful or meet some requirement.[51] This occurs in REM sleep rather than in NREM sleep.[52][53] Rather than being due to memory processes, this has been attributed to changes during REM sleep in cholinergic and noradrenergic neuromodulation.[52] High levels of acetylcholine in the hippocampus suppress feedback from hippocampus to the neocortex, while lower levels of acetylcholine and norepinephrine in the neocortex encourage the uncontrolled spread of associational activity within neocortical areas.[54] This is in contrast to waking consciousness, where higher levels of norepinephrine and acetylcholine inhibit recurrent connections in the neocortex. REM sleep through this process adds creativity by allowing "neocortical structures to reorganise associative hierarchies, in which information from the hippocampus would be reinterpreted in relation to previous semantic representations or nodes."[52]


Sample hypnogram (electroencephalogram of sleep) showing sleep cycles characterized by increasing paradoxical (REM) sleep.

In the ultradian sleep cycle an organism alternates between deep sleep (slow, large, synchronized brain waves) and paradoxical sleep (faster, desynchronized waves). Sleep happens in the context of the larger circadian rhythm, which influences sleepiness and physiological factors based on timekeepers within the body. Sleep can be distributed throughout the day or clustered during one part of the rhythm: in nocturnal animals, during the day, and in diurnal animals, at night.[55] The organism returns to homeostatic regulation almost immediately after REM sleep ends.[56]

During a night of sleep, one usually experiences about four or five periods of REM sleep; they are quite short at the beginning of the night and longer toward the end. Many animals and some people tend to wake, or experience a period of very light sleep, for a short time immediately after a bout of REM. The relative amount of REM sleep varies considerably with age. A newborn baby spends more than 80% of total sleep time in REM.[57] During REM, the activity of the brain's neurons is quite similar to that during waking hours; for this reason, the REM-sleep stage may be called paradoxical sleep.[58]

REM sleep typically occupies 20–25% of total sleep in adult humans: about 90–120 minutes of a night's sleep. The first REM episode occurs about 70 minutes after falling asleep. Cycles of about 90 minutes each follow, with each cycle including a larger proportion of REM sleep.[15]

Infants spend more time in higher REM sleep than adults. The proportion of REM sleep then decreases significantly in childhood. Older people tend to sleep less overall but sleep in REM for about the same absolute time, and therefore spend a greater proportion of sleep in REM.[59]

Rapid eye movement sleep can be subclassified into tonic and phasic modes.[60] Tonic REM is characterized by theta rhythms in the brain; phasic REM is characterized by PGO waves and actual “rapid” eye movements. Processing of external stimuli is heavily inhibited during phasic REM and recent evidence suggests that sleepers are more difficult to arouse from phasic REM than in slow-wave sleep.[7]

Effects of REM sleep deprivation

REM deprivation causes a significant increase in the number of attempts to go into REM stage while asleep. On recovery nights, an individual will most likely move to stage 3 and REM sleep more quickly and experience an REM rebound, which refers to a great increase in the time spent in REM stage over normal levels. These findings are consistent with the idea that REM sleep is biologically necessary.[61][62]

After the deprivation is complete, mild psychological disturbances, such as anxiety, irritability, hallucinations, and difficulty concentrating may develop and appetite may increase. There are also positive consequences of REM deprivation. Some symptoms of depression are found to be suppressed by REM deprivation; aggression, and eating behavior may increase.[62][63] Higher noradrenaline is a possible cause of these results.[10] Whether and how long-term REM deprivation has psychological effects remains a matter of controversy. Several reports have indicated that REM deprivation increases aggressive and sexual behavior in laboratory test animals.[62]

It has been suggested that acute REM sleep deprivation can improve certain types of depression when depression appears to be related to an imbalance of certain neurotransmitters. Although sleep deprivation in general annoys most of the population, it has repeatedly been shown to alleviate depression, albeit temporarily.[64] More than half the individuals who experience this relief report it to be rendered ineffective after sleeping the following night. Thus, researchers have devised methods such as altering the sleep schedule for a span of days following a REM deprivation period[65] and combining sleep-schedule alterations with pharmacotherapy[66] to prolong this effect. Though most antidepressants selectively inhibit REM sleep due to their action on monoamines, this effect decreases after long-term use. Sleep deprivation stimulates hippocampal neurogenesis much the same as antidepressants, but whether this effect is driven by REM sleep in particular is unknown.[67]

Animal studies of REM deprivation are markedly different from human studies. There is evidence that REM sleep deprivation in animals has more serious consequences than in humans. This may be because the length of time animals have been REM deprived for is much longer (up to seventy days) or because the various experimental protocols used have been more uncomfortable and painful than those for humans.[63] The “flower pot” method involves placing a laboratory animal above water on a platform so small that it falls off upon losing muscle tone. The naturally rude awakening which results may elicit changes in the organism which necessarily exceed the simple absence of a sleep phase.[68] Another method involves computer monitoring of brain waves, complete with automatic mechanized shaking of the cage when the test animal drifts into REM sleep.[69]

Evidence suggests that REM deprivation in rats impairs learning of new material, but does not affect existing memory. In one study, rats did not learn to avoid a painful stimulus after REM deprivation as well as they could before the deprivation. No learning impairments have been found in humans undergoing one night of REM deprivation. REM deprivation in rats produces an increase in attempts to enter REM, and after deprivation, REM rebound. In rats, as well as cats, REM sleep deprivation increased brain excitability (e.g. electrical amplification of sensory signals), and which lowered the threshold for waking seizures threshold. This increase in brain excitability seems to be similar in humans. One study also found a decrease in hindbrain sensory excitability. The hindbrain was less receptive overall to information in the afferent pathway, because of the increase in the amplification of those pathways that it is receptive to.[63]

REM sleep in animals

Ostriches sleeping, with REM and slow-wave sleep phases.[70]
Rapid eye movement of a dog

REM sleep occurs in all land mammals as well as in birds. Amount of REM sleep and cycling time vary among animals; predators enjoy more REM sleep than prey.[10] Larger animals also tend to stay in REM for longer, possibly because higher thermal inertia of their brains and bodies allows them to tolerate longer suspension of thermoregulation.[71] The period (full cycle of REM and non-REM) lasts for about 90 minutes in humans, 22 minutes in cats, and 12 minutes in rats.[72]

In utero, mammals spend more than half (50–80%) of a 24-hour day in REM sleep.[15]

Hypotheses about the function(s) of REM sleep

While the function of REM sleep is not well understood, several theories have been proposed.


Sleep in general seems to aid memory. REM sleep may favor the preservation of certain types of memories: specifically, procedural memory, spatial memory, and emotional memory. REM sleep seems to increase following intensive learning in rats, especially several hours after, and sometimes for multiple nights after. Experimental REM deprivation has sometimes inhibited memory consolidation, especially regarding complex processes (e.g., how to escape from an elaborate maze).[73] In humans, the best evidence for REMS improvement of memory pertains to learning of procedures—new ways of moving the body (such as trampoline jumping), and new techniques of problem solving. REM deprivation seemed to impair declarative (i.e., factual) memory only in more complex cases, such as memories of longer stories.[74] REM sleep apparently counteracts attempts to suppress certain thoughts.[50]

According to the dual-process hypothesis of sleep and memory, the two major phases of sleep correspond to different types of memory. “Night half” studies have tested this hypothesis with memory tasks either begun before sleep and assessed in the middle of the night, or begun in the middle of the night and assessed in the morning.[75] Slow-wave sleep, part of non-REM sleep, appears to be important for declarative memory. Artificial enhancement of the non-REM sleep improves the next-day recall of memorized pairs of words.[76] Tucker et al. demonstrated that a daytime nap containing solely non-REM sleep enhances declarative memory but not procedural memory.[77] According to the sequential hypothesis the two types of sleep work together to consolidate memory.[78]

Monoamine oxidase (MAO) inhibitors and tricyclic antidepressants can suppress REM sleep and these drugs show no evidence of impairing memory. Some studies show MAO inhibitors improve memory. Moreover, one case study of an individual who had little or no REM sleep due to a shrapnel injury to the brainstem did not find the individual's memory to be impaired. (For a more detailed critique on the link between sleep and memory, see Ref.)[79])

Intimately related to views on REM function in memory consolidation, Graeme Mitchison and Francis Crick have proposed in 1983 that by virtue of its inherent spontaneous activity, the function of REM sleep "is to remove certain undesirable modes of interaction in networks of cells in the cerebral cortex", which process they characterize as "unlearning". As a result, those memories which are relevant (whose underlying neuronal substrate is strong enough to withstand such spontaneous, chaotic activation), are further strengthened, whilst weaker, transient, "noise" memory traces disintegrate.[80] Memory consolidation during paradoxical is specifically correlated with the periods of rapid eye movement, which do not occur continuously. One explanation for this correlation is that the PGO electrical waves, which precede the eye movements, also influence memory.[6] REM sleep could provide a unique opportunity for “unlearning” to occur in basic neural networks involved in homeostasis, which are protected from this “synaptic downscaling” effect during deep sleep.[81]

Stimulation of the central nervous system's development as a primary function

According to another theory, known as the Ontogenetic Hypothesis of REM sleep, this sleep stage (also known as active sleep in neonates) is particularly important to the developing brain, possibly because it provides the neural stimulation that newborns need to form mature neural connections and for proper nervous system development.[82] Studies investigating the effects of active sleep deprivation have shown that deprivation early in life can result in behavioral problems, permanent sleep disruption, decreased brain mass,[83] and result in an abnormal amount of neuronal cell death.[84] Further supporting this theory is the fact that the amount of REM sleep in humans decreases with age, as well as data from other species (see below).

One important theoretical consequence of the Ontogenetic Hypothesis is that REM sleep may have no essentially vital function in the mature brain, i.e., once the development of the central nervous system has completed. However, because processes of neuronal plasticity do not cease altogether in the brain,[85] REM sleep may continue to be implicated in neurogenesis in adults as a source of sustained spontaneous stimulation.

Defensive immobilization: the precursor of dreams

According to Tsoukalas (2012) REM sleep is an evolutionary transformation of a well-known defensive mechanism, the tonic immobility reflex. This reflex, also known as animal hypnosis or death feigning, functions as the last line of defense against an attacking predator and consists of the total immobilization of the animal so that it appears dead. Tsoukalas argues that the neurophysiology and phenomenology of this reaction shows striking similarities to REM sleep; for example, both reactions exhibit brainstem control, paralysis, sympathetic activation, and thermoregulatory changes.[86][87]

Shift of gaze

According to "scanning hypothesis", the directional properties of REM sleep are related to a shift of gaze in dream imagery. Against this hypothesis is that such eye movements occur in those born blind and in fetuses in spite of lack of vision. Also, binocular REMs are non-conjugated (i.e., the two eyes do not point in the same direction at a time) and so lack a fixation point. In support of this theory, research finds that in goal-oriented dreams, eye gaze is directed towards the dream action, determined from correlations in the eye and body movements of REM sleep behavior disorder patients who enact their dreams.[88]

Oxygen supply to cornea

Dr. David M. Maurice (1922-2002), an eye specialist and retired professor at Columbia University, proposed that REM sleep was associated with oxygen supply to cornea when the animal was sleeping thus aqueous humor, the liquid between cornea and iris, was stagnant if not stirred ("stagnant aqueous humor hypothesis").[89] Among the supportive evidences, He calculated that if aqueous humor was stagnant, oxygen from iris had to reach cornea by diffusion through aqueous humor, which was not sufficient. According to the theory, when the animal is awake, eye movement and/or cool environmental temperature make sure the aqueous humor is able to circulate. When the animal is sleeping, REM provides the much needed stir to aqueous humor. This theory is consistent with the observation that fetuses, as well as eye-sealed newborn animals, spend much time in REM sleep, and that during a normal sleep, a person's REM sleep episodes become progressively longer deeper into the night. However, owls have REM sleep (telling from EEG recording) but during REM sleep owls do not move their head more than Non-REM sleep. This observation can be derived from Figure S1 of a recently published research [90] and it is well known that owls can not roll their eyes.

Other theories

Another theory suggests that monoamine shutdown is required so that the monoamine receptors in the brain can recover to regain full sensitivity. Indeed, if REM sleep is repeatedly interrupted, the person will compensate for it with longer REM sleep, "rebound sleep", at the next opportunity.

Some researchers argue that the perpetuation of a complex brain process such as REM sleep indicates that it serves an important function for the survival of mammalian and avian species. It fulfills important physiological needs vital for survival to the extent that prolonged REM sleep deprivation leads to death in experimental animals. In both humans and experimental animals, REM sleep loss leads to several behavioral and physiological abnormalities. Loss of REM sleep has been noticed during various natural and experimental infections. Survivability of the experimental animals decreases when REM sleep is totally attenuated during infection; this leads to the possibility that the quality and quantity of REM sleep is generally essential for normal body physiology.[91]

The sentinel hypothesis of REM sleep was put forward by Frederick Snyder in 1966. It is based upon the observation that REM sleep in several mammals (the rat, the hedgehog, the rabbit, and the rhesus monkey) is followed by a brief awakening. This does not occur for either cats or humans, although humans are more likely to wake from REM sleep than from NREM sleep. Snyder hypothesized that REM sleep activates an animal periodically, to scan the environment for possible predators. This hypothesis does not explain the muscle paralysis of REM sleep; however, a logical analysis might suggest that the muscle paralysis exists to prevent the animal from fully waking up unnecessarily, and allowing it to return easily to deeper sleep.[92][93][94]

Jim Horne, a sleep researcher at Loughborough University, has suggested that REM in modern humans compensates for the reduced need for wakeful food foraging.[1]

Other theories are that they lubricate the cornea, warm the brain, stimulate and stabilize the neural circuits that have not been activated during waking, create internal stimulation to aid development of the CNS, or lack any purpose, being random creations of brain activation.[88][95]

Discovery and further research

The German scientist Richard Klaue in 1937 first discovered a period of fast electrical activity in the brains of sleeping cats. In 1944, Ohlmeyer reported 90-minute ultradian sleep cycles involving male erections lasting for 25 minutes.[96] At University of Chicago in 1952, Eugene Aserinsky, Nathaniel Kleitman, and William C. Dement, discovered phases of rapid eye movement during sleep, and connected these to dreaming. Their article was published September 10, 1953.[97]

William Dement advanced the study of REM deprivation, with experiments in which subjects were awoken every time their EEG indicated the beginning of REM sleep. He published "The Effect of Dream Deprivation" in June 1960.[98] ("REM deprivation" has become the more common term following subsequent research indicating the possibility of non-REM dreaming.)

Neurosurgical experiments by Michel Jouvet and others in the following two decades added an understanding of atonia and suggested the importance of the pontine tegmentum (dorsolateral pons) in enabling and regulating paradoxical sleep.[10] Jouvet and others found that damaging the reticular formation of the brainstem inhibited this type of sleep.[34] Jouvet coined the name “paradoxical sleep” in 1959 and in 1962 published results indicating that it could occur in a cat with its entire forebrain removed.[14][95]

See also


  1. 1.0 1.1 Jim Horne (2013), “Why REM sleep? Clues beyond the laboratory in a more challenging world”, Biological Psychology 92.
  2. Steriade & McCarley (1990), Brainstem Control of Wakefulness and Sleep", §8.1 (pp. 232–243).
  3. Jayne Gackenbach, “Interhemispheric EEG Coherence in REM Sleep and Meditation: The Lucid Dreaming Connection” in Antrobus & Bertini (eds.), The Neuropsychology of Sleep and Dreaming.
  4. Steriade & McCarley (1990), Brainstem Control of Wakefulness and Sleep", §9.1–2 (pp. 263–282).
  5. Steriade & McCarley (1990), Brainstem Control of Wakefulness and Sleep", §1.2 (pp. 7–23).
  6. 6.0 6.1 6.2 Subimal Datta (1999), "PGO Wave Generation: Mechanism and functional significance", in Rapid Eye Movement Sleep ed. Mallick & Inoué.
  7. 7.0 7.1 7.2 Ummehan Ermis, Karsten Krakow, & Ursula Voss (2010), “Arousal thresholds during human tonic and phasic REM sleep”, Journal of Sleep Research 19.
  8. 8.0 8.1 8.2 8.3 8.4 8.5 8.6 J. Alan Hobson, Edward F. Pace-Scott, & Robert Stickgold (2000), “Dreaming and the brain: Toward a cognitive neuroscience of conscious states”, Behavioral and Brain Sciences 23.
  9. 9.0 9.1 9.2 Ritchie E. Brown & Robert W. McCarley (2008), "Neuroanatomical and neurochemical basis of wakefulness and REM sleep systems", in Neurochemistry of Sleep and Wakefulness ed. Monti et al.
  10. 10.0 10.1 10.2 10.3 10.4 Birendra N. Mallick, Vibha Madan, & Sushil K. Jha (2008), "Rapid eye movement sleep regulation by modulation of the noradrenergic system", in Neurochemistry of Sleep and Wakefulness ed. Monti et al.
  11. 11.0 11.1 Hobson JA (2009). "REM sleep and dreaming: towards a theory of protoconsciousness". Nature Reviews. 10 (11): 803–813. doi:10.1038/nrn2716. PMID 19794431.<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  12. 12.0 12.1 Aston-Jones G., Gonzalez M., & Doran S. (2007). "Role of the locus coeruleus-norepinephrine system in arousal and circadian regulation of the sleep-wake cycle." Ch. 6 in Brain Norepinephrine: Neurobiology and Therapeutics. G.A. Ordway, M.A. Schwartz, & A. Frazer, eds. Cambridge UP. 157–195. Accessed 21 Jul. 2010. Academicdepartments.musc.edu
  13. Siegel J.M. (2005). "REM Sleep." Ch. 10 in Principles and Practice of Sleep Medicine. 4th ed. M.H. Kryger, T. Roth, & W.C. Dement, eds. Elsevier. 120–135.
  14. 14.0 14.1 14.2 Pierre-Hervé Luppi et al. (2008), "Gamma-aminobutyric acid and the regulation of paradoxical, or rapid eye movement, sleep", in Neurochemistry of Sleep and Wakefulness ed. Monti et al.
  15. 15.0 15.1 15.2 Robert W. McCarley (2007), “Neurobiology of REM and NREM sleep”, Sleep Medicine 8.
  16. 16.0 16.1 J. Alan Hobson & Robert W. McCarley, “The Brain as a Dream-State Generator: An Activation-Synthesis Hypothesis of the Dream Process”, American Journal of Psychiatry 134.12, December 1977.
  17. Steriade & McCarley (1990), Brainstem Control of Wakefulness and Sleep", §12.2 (pp. 369–373).
  18. Ralph Lydic & Helen A. Baghdoyan, "Acetylcholine modulates sleep and wakefulness: a synaptic perspective", in Neurochemistry of Sleep and Wakefulness ed. Monti et al.
  19. Parmeggiani (2011), Systemic Homeostasis and Poikilostasis in Sleep, p. 16.
  20. Steriade & McCarley (1990), Brainstem Control of Wakefulness and Sleep", §10.7.2 (pp. 307–309).
  21. Parmeggiani (2011), Systemic Homeostasis and Poikilostasis in Sleep, p. 12–15.
  22. Parmeggiani (2011), Systemic Homeostasis and Poikilostasis in Sleep, p. 22–27.
  23. Parmeggiani (2011), Systemic Homeostasis and Poikilostasis in Sleep, p. 35–37
  24. Jouvet (1999), The Paradox of Sleep, pp. 169–173.
  25. Brown et al. (2012), “Control of Sleep and Wakefulness”, p. 1127.
  26. Parmeggiani (2011), Systemic Homeostasis and Poikilostasis in Sleep, p. 12–13.
  27. Parmeggiani (2011), Systemic Homeostasis and Poikilostasis in Sleep, pp. 46–47.
  28. Parmeggiani (2011), Systemic Homeostasis and Poikilostasis in Sleep, pp. 51–52.
  29. Ronald Szymusiak, Md. Noor Alam, & Dennis McGinty (1999), "Thermoregulatory Control of the NonREM-REM Sleep Cycle", in Rapid Eye Movement Sleep ed. Mallick & Inoué.
  30. Parmeggiani (2011), Systemic Homeostasis and Poikilostasis in Sleep, pp. 57–59.
  31. Parmeggiani (2011), Systemic Homeostasis and Poikilostasis in Sleep, p. 45. “Therefore, it appears that the onset of REM sleep requires the inactivation of the central thermostat in late NREM sleep. However, only a restricted range of preoptic-hypothalamic temperatures at the end of NREM sleep is compatible with REM sleep onset. This range may be considered a sort of temperature gate for REM sleep, that is constrained in width more at low than at neutral ambient temperature.”
  32. Parmeggiani (2011), Systemic Homeostasis and Poikilostasis in Sleep, p. 61. “On the other hand, a balance between opposing ambient and preoptic-anterior hypothalamic thermal loads influencing peripheral and central thermoreceptors, respectively, may be experimentally achieved so as to promote sleep. In particular, warming of the preoptic-anterior hypothalamic region in a cold environment hastens REM sleep onset and increases its duration (Parmeggiana et al., 1974, 1980; Sakaguchi et al., 1979).”
  33. Steriade & McCarley (1990), Brainstem Control of Wakefulness and Sleep", §10.8–9 (pp. 309–324).
  34. 34.0 34.1 Yuan-Yang Lai & Jerome M. Siegel (1999), "Muscle Atonia in REM Sleep", in Rapid Eye Movement Sleep ed. Mallick & Inoué.
  35. Parmeggiani (2011), Systemic Homeostasis and Poikilostasis in Sleep, p. 17. “In other words, the functional controls requiring high hierarchical levels of integration are the most affected during REM sleep, whereas reflex activity is only altered but not obliterated.”
  36. Lapierre O, Montplaisir J (1992). "Polysomnographic features of REM sleep behavior disorder: development of a scoring method". Neurology. 42 (7): 1371–4. doi:10.1212/wnl.42.7.1371. PMID 1620348.<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  37. Steriade & McCarley (1990), Brainstem Control of Wakefulness and Sleep", § (pp. 428–432).
  38. Jouvet (1999), The Paradox of Sleep, p. 102.
  39. Steriade & McCarley (1990), Brainstem Control of Wakefulness and Sleep", §13.1 (pp. 396–400).
  40. Steriade & McCarley (1990), Brainstem Control of Wakefulness and Sleep", §13.2 (pp. 400–415).
  41. Koval'zon VM (Jul–Aug 2011). "[Central mechanisms of sleep-wakefulness cycle]". Fiziologiia cheloveka. 37 (4): 124–34. PMID 21950094.<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  42. "[Polysomnography]". Retrieved 2 November 2011.<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  43. Parmeggiani (2011), Systemic Homeostasis and Poikilostasis in Sleep, p. 87. “The open-loop mode of physiological regulation in REM sleep may restore the efficiency of the different neuronal networks of the brain stem by expressing also genetically coded patterns of instinctive behavior that are kept normally hidden from view by skeletal muscle atonia. Such behaviorally concealed neuronal activity was demonstrated by the effects of experimental lesions of specific pontine structures (Hendricks, 1982; Hendricks et al., 1977, 1982; Henley and Morrison, 1974; Jouvet and Delorme, 1965; Sastre and Jouvet, 1979; Villablanca, 1996). Not only was the skeletal muscle atonia suppressed by also motor fragments of complex instinctive behaviors appeared, such as walking and attack, that were not externally motivated (see Morrison, 2005).”
  44. Solms (1997), The Neuropsychology of Dreams, pp. 10, 34.
  45. 45.0 45.1 45.2 45.3 Ruth Reinsel, John Antrobus, & Miriam Wollman (1992), “Bizarreness in Dreams and Waking Fantasy”, in Antrobus & Bertini (eds.), The Neuropsychology of Sleep and Dreaming.
  46. Stephen LaBerge (1992), “Physiological Studies of Lucid Dreaming”, in Antrobus & Bertini (eds.), The Neuropsychology of Sleep and Dreaming.
  47. Delphine Ouidette et al. (2012), “Dreaming without REM sleep”, Consciousness and Cognition 21.
  48. Solms (1997), The Neuropsychology of Dreams, Chapter 6: “The Problem of REM Sleep” (pp. 54–57).”
  49. Jouvet (1999), The Paradox of Sleep, p. 104. “I frankly support the theory that we do not dream all night, as do William Dement and Alan Hobson and most neurophysiologists. I am rather surprised that publications about dream recall during slow wave sleep increase in number each year. Further, the classic distinction established in the 1960s between 'poor' dream recall, devoid of color and detail, during slow wave sleep, and 'rich' recall, full of color and detail, during paradoxical sleep, is beginning to disappear. I believe that dream recall during slow wave sleep could be recall from previous paradoxical sleep.”
  50. 50.0 50.1 Rasch & Born (2013), “About Sleep's Role in Memory”, p. 688.
  51. Wagner U, Gais S, Haider H, Verleger R, Born J (2004). "Sleep inspires insight". Nature. 427 (6972): 352–5. doi:10.1038/nature02223. PMID 14737168.CS1 maint: multiple names: authors list (link)<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  52. 52.0 52.1 52.2 Cai DJ, Mednick SA, Harrison EM, Kanady JC, Mednick SC (2009). "REM, not incubation, improves creativity by priming associative networks". Proc Natl Acad Sci U S A. 106 (25): 10130–10134. doi:10.1073/pnas.0900271106. PMC 2700890. PMID 19506253.CS1 maint: multiple names: authors list (link)<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  53. Walker MP, Liston C, Hobson JA, Stickgold R (November 2002). "Cognitive flexibility across the sleep-wake cycle: REM-sleep enhancement of anagram problem solving". Brain research. Cognitive brain research. 14 (3): 317–24. doi:10.1016/S0926-6410(02)00134-9. PMID 12421655.CS1 maint: multiple names: authors list (link)<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  54. Hasselmo ME (September 1999). "Neuromodulation: acetylcholine and memory consolidation". Trends in cognitive sciences. 3 (9): 351–359. doi:10.1016/S1364-6613(99)01365-0. PMID 10461198.<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  55. Parmeggiani (2011), Systemic Homeostasis and Poikilostasis in Sleep, p. 9–11.
  56. Parmeggiani (2011), Systemic Homeostasis and Poikilostasis in Sleep, p. 17.
  57. Van Cauter E, Leproult R, Plat L (2000). "Age-related changes in slow wave sleep and REM sleep and relationship with growth hormone and cortisol levels in healthy men". JAMA. 284 (7): 861–8. doi:10.1001/jama.284.7.861. PMID 10938176.CS1 maint: multiple names: authors list (link)<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  58. Myers, David (2004). Psychology (7th ed.). New York: Worth Publishers. p. 268. ISBN 0-7167-8595-1. Retrieved 2010-01-09.<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  59. Kazuo Mishima, Tetsuo Shimizu, & Yasuo Hishikawa (1999), "REM Sleep Across Age and Sex", in Rapid Eye Movement Sleep ed. Mallick & Inoué.
  60. Kryger M, Roth T, Dement W (2000). Principles & Practices of Sleep Medicine. WB Saunders Company. pp. 1, 572.CS1 maint: multiple names: authors list (link)<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  61. Endo T, Roth C, Landolt HP, Werth E, Aeschbach D, Achermann P, Borbély AA (1998). "Selective REM sleep deprivation in humans: Effects on sleep and sleep EEG". The American journal of physiology. 274 (4 Pt 2): R1186–R1194. PMID 9575987.CS1 maint: multiple names: authors list (link)<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  62. 62.0 62.1 62.2 Steven J. Ellman, Arthur J. Spielman, Dana Luck, Solomon S. Steiner, & Ronnie Halperin (1991), "REM Deprivation: A Review", in The Mind in Sleep, ed. Ellman & Antrobus.
  63. 63.0 63.1 63.2 "Types of Sleep Deprivation".<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  64. Ringel BL, Szuba MP (2001). "Potential mechanisms of the sleep therapies for depression". Depression and Anxiety. 14 (1): 29–36. doi:10.1002/da.1044. PMID 11568980.<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  65. Riemann D, König A, Hohagen F, Kiemen A, Voderholzer U, Backhaus J, Bunz J, Wesiack B, Hermle L, Berger M (1999). "How to preserve the antidepressive effect of sleep deprivation: A comparison of sleep phase advance and sleep phase delay". European Archives of Psychiatry and Clinical Neuroscience. 249 (5): 231–237. doi:10.1007/s004060050092. PMID 10591988.CS1 maint: multiple names: authors list (link)<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  66. Wirz-Justice A, Van den Hoofdakker RH (1999). "Sleep deprivation in depression: What do we know, where do we go?". Biological Psychiatry. 46 (4): 445–453. doi:10.1016/S0006-3223(99)00125-0. PMID 10459393.<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  67. Grassi Zucconi G, Cipriani S, Balgkouranidou I, Scattoni R (2006). "'One night' sleep deprivation stimulates hippocampal neurogenesis". Brain Research Bulletin. 69 (4): 375–381. doi:10.1016/j.brainresbull.2006.01.009. PMID 16624668.CS1 maint: multiple names: authors list (link)<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  68. Rasch & Born (2013), “About Sleep's Role in Memory”, p. 686–687.
  69. Pingfu Feng, Yuxian Ma, & Gerald W. Vogel (2001), “Ontogeny of REM Rebound in Postnatal Rats”, SLEEP 24.6.
  70. Lesku, J. A.; Meyer, L. C. R.; Fuller, A.; Maloney, S. K.; Dell'Omo, G.; Vyssotski, A. L.; Rattenborg, N. C. (2011). Balaban, Evan (ed.). "Ostriches Sleep like Platypuses". PLoS ONE. 6 (8): e23203. doi:10.1371/journal.pone.0023203. PMC 3160860. PMID 21887239.<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  71. Parmeggiani (2011), Systemic Homeostasis and Poikilostasis in Sleep, pp. 13, 59–61. “In species with different body mass (e.g., rats, rabbits, cats, humans) the average duration of REM sleep episodes increases with the increase in body and brain weight, a determinant of the thermal inertia. Such inertia delays the changes in body core temperature so alarming as to elicit arousal from REM sleep. In addition, other factors, such as fur, food, and predator–prey relationships influencing REM sleep duration out to be mentioned here.”
  72. Steriade & McCarley (1990), Brainstem Control of Wakefulness and Sleep", §12.1 (p. 363).
  73. Rasch & Born (2013), “About Sleep's Role in Memory”, p. 686. Deprivation of REM sleep (mostly without simultaneous sleep recording) appeared to primarily impair memory for- mation on complex tasks, like two-way shuttle box avoidance and complex mazes, which encompass a change in the animals regular repertoire (69, 100, 312, 516, 525, 539, 644, 710, 713, 714, 787, 900, 903–906, 992, 1021, 1072, 1111, 1113, 1238, 1352, 1353). In contrast, long-term memory for simpler tasks, like one-way active avoidance and simple mazes, were less consistently affected (15, 249, 386, 390, 495, 558, 611, 644, 821, 872, 902, 907–909, 1072, 1091, 1334).”
  74. Rasch & Born (2013), “About Sleep's Role in Memory”, p. 687.
  75. Rasch & Born (2013), “About Sleep's Role in Memory”, p. 689. “The dual process hypothesis assumes that different sleep stages serve the consolidation of different types of memories (428, 765, 967, 1096). Specifically it has been assumed that declarative memory profits from SWS, whereas the consolidation of nondeclarative memory is supported by REM sleep.” This hypothesis received support mainly from studies in humans, particularly from those employing the 'night half paradigm.'”
  76. Marshall L, Helgadóttir H, Mölle M, Born J (2006). "Boosting slow oscillations during sleep potentiates memory". Nature. 444 (7119): 610–3. doi:10.1038/nature05278. PMID 17086200.CS1 maint: multiple names: authors list (link)<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  77. Tucker MA, Hirota Y, Wamsley EJ, Lau H, Chaklader A, Fishbein W (2006). "A daytime nap containing solely non-REM sleep enhances declarative but not procedural memory" (PDF). Neurobiology of Learning and Memory. Elsevier. 86 (2): 241–7. doi:10.1016/j.nlm.2006.03.005. PMID 16647282. Retrieved June 29, 2011.CS1 maint: multiple names: authors list (link)<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  78. Rasch & Born (2013), “About Sleep's Role in Memory”, p. 690–691.
  79. Siegel, Jerome M. "The REM Sleep-Memory Consolidation Hypothesis". Cite journal requires |journal= (help)<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  80. Crick F, Mitchison G (1983). "The function of dream sleep". Nature. 304 (5922): 111–14. doi:10.1038/304111a0. PMID 6866101.<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  81. Parmeggiani (2011), Systemic Homeostasis and Poikilostasis in Sleep, p. 89. “In contrast to NREM sleep, downscaling of synapses would be produced in REM sleep by random bursts of neuronal firing (e.g., also bursts underlying ponto-geniculo-occipital waves) (see Tonioni and Cirelli, 2005). / This hypothesis is particularly enriched in functional significance by considering at this point the opposite nature, homeostatic and poikilostatic, of the systemic neural regulation of physiological functions in these sleep states. The important fact is that homeostasis if fully preserved in NREM sleep. This means that a systemic synaptic downcaling (slow-wave electroencephalographic activity) is practically limited to the relatively homogenous cortical structures of the telencephalon, while the whole brain stem, from diencephalon to medulla, is still exerting its basic functions of integrated homeostatic regulation of both somatic and autonomic physiological functions. In REM sleep, however, the necessary synaptic downscaling in the brain stem is instead the result of random neuronal firing.”
  82. Marks et al. 1994
  83. Mirmiran M, Scholtens J, van de Poll NE, Uylings HB, van der Gugten J, Boer GJ (1983). "Effects of experimental suppression of active (REM) sleep during early development upon adult brain and behavior in the rat". Brain Res. 283 (2–3): 277–86. doi:10.1016/0165-3806(83)90184-0. PMID 6850353.CS1 maint: multiple names: authors list (link)<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  84. Morrissey MJ, Duntley SP, Anch AM, Nonneman R (2004). "Active sleep and its role in the prevention of apoptosis in the developing brain". Med. Hypotheses. 62 (6): 876–9. doi:10.1016/j.mehy.2004.01.014. PMID 15142640.CS1 maint: multiple names: authors list (link)<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  85. Bruel-Jungerman E, Rampon C, Laroche S (2006). "Adult hippocampal neurogenesis, synaptic plasticity and memory: facts and hypotheses". Rev. Neurosci. 18 (2): 93–114. doi:10.1515/REVNEURO.2007.18.2.93. PMID 17593874.CS1 maint: multiple names: authors list (link)<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  86. Tsoukalas I (2012). "The origin of REM sleep: A hypothesis". Dreaming. 22 (4): 253–283. doi:10.1037/a0030790.<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  87. Vitelli, R. (2013). Exploring the Mystery of REM Sleep. Psychology Today, On-line, March 25
  88. 88.0 88.1 Leclair-Visonneau L, Oudiette D, Gaymard B, Leu-Semenescu S, Arnulf I (2010). "Do the eyes scan dream images during rapid eye movement sleep? Evidence from the rapid eye movement sleep behaviour disorder model". Brain. 133 (6): 1737–46. doi:10.1093/brain/awq110. PMID 20478849.CS1 maint: multiple names: authors list (link)<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  89. Maurice, David (1998). "The Von Sallmann Lecture 1996: An Ophthalmological Explanation of REM Sleep" (PDF). Experimental Eye Research. 66 (2): 139–145. doi:10.1006/exer.1997.0444. PMID 9533840.<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  90. Madeleine Scriba, Anne-Lyse Ducrest, Isabelle Henry, Alexei L Vyssotski, Niels C Rattenborg and Alexandre Roulin (2013). "Linking melanism to brain development: expression of a melanism-related gene in barn owl feather follicles covaries with sleep ontogeny". Frontiers in Zoology. 10 (42). doi:10.1186/1742-9994-10-42.CS1 maint: multiple names: authors list (link)<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  91. Robert P. Vertes (1986), "A Life-Sustaining Function for REM Sleep: A Theory", Neuroscience and Behavioral Reviews 10.
  92. Steven J. Ellman and John S. Antrobus (1991). "Effects of REM deprivation". The Mind in Sleep: Psychology and Psychophysiology. John Wiley and Sons. p. 398. ISBN 0-471-52556-1.<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  93. Jouvet (1999), The Paradox of Sleep, pp. 122–124.
  94. William H. Moorcroft and Paula Belcher (2003). "Functions of REMS and Dreaming". Understanding Sleep and sDreaming. Springer. p. 290. ISBN 0-306-47425-5.<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  95. 95.0 95.1 Perrine M. Ruby (2011), “Experimental research on dreaming: state of the art and neuropsychoanalytic perspectives”, Frontiers in Psychology 2.
  96. Jouvet (1999), The Paradox of Sleep, p. 32.
  97. Aserinsky E, Kleitman N (1953). "Regularly Occurring Periods of Eye Motility, and Concomitant Phenomena, during Sleep". Science. 118 (3062): 273–274. doi:10.1126/science.118.3062.273. PMID 13089671.<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  98. William Dement, “The Effect of Dream Deprivation: The need for a certain amount of dreaming each night is suggested by recent experiments.” Science 131.3415, 10 June 1960.


  • Antrobus, John S., & Mario Bertini (1992). The Neuropsychology of Sleep and Dreaming. Hillsdale, NJ: Lawrence Erlbaum Associates. ISBN 0-8058-0925-2
  • Brown, Ritchie E., Radhika Basheer, James T. McKenna, Robert E. Strecker, & Robert W. McCarley (2012). “Control of Sleep and Wakefulness”. Physiological Review 92, pp. 1087–1187.
  • Ellman, Steven J., & Antrobus, John S. (1991). The Mind in Sleep: Psychology and Psychophysiology. Second edition. John Wiley & Sons, Inc. ISBN 0-471-52556-1
  • Jouvet, Michel (1999). The Paradox of Sleep: The Story of Dreaming. Originally Le Sommeil et le Rêve, 1993. Translated by Laurence Garey. Cambridge: MIT Press. ISBN 0-262-10080-0
  • Mallick, B. N., & S. Inoué (1999). Rapid Eye Movement Sleep. New Delhi: Narosa Publishing House; distributed in the Americas, Europe, Australia, & Japan by Marcel Dekker Inc (New York).
  • Monti, Jaime M., S. R. Pandi-Perumal, & Christopher M. Sinton (2008). Neurochemistry of Sleep and Wakefulness. Cambridge University Press. ISBN 978-0-521-86441-1
  • Parmeggiani, Pier Luigi (2011). Systemic Homeostasis and Poikilostasis in Sleep: Is REM Sleep a Physiological Paradox? London: Imperial College Press. ISBN 978-1-94916-572-2
  • Rasch, Björn, & Jan Born (2013). “About Sleep's Role in Memory”. Physiological Review 93, pp. 681–766.
  • Solms, Mark (1997). The Neuropsychology of Dreams: A Clinico-Anatomical Study. Mahwah, NJ: Lawrence Erlbaum Associates; ISBN 0-8058-1585-6
  • Steriade, Mircea, & Robert W. McCarley (1990). Brainstem Control of Wakefulness and Sleep. New York: Plenum Press. ISBN 0-306-43342-7

Further reading

  • Snyder F (1966). "Toward an Evolutionary Theory of Dreaming". American Journal of Psychiatry. 123 (2): 121–142. doi:10.1176/ajp.123.2.121. PMID 5329927.<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  • Edward F. Pace-Schott, ed. (2003). Sleep and Dreaming: Scientific Advances and Reconsiderations. Cambridge University Press. ISBN 0-521-00869-7.<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  • Koulack, D. To Catch A Dream: Explorations of Dreaming. New York, SUNY, 1991.
  • Nguyen TQ, Liang CL, Marks GA (2013). "GABA(A) receptors implicated in REM sleep control express a benzodiazepine binding site". Brain Res. 1527: 131–40. doi:10.1016/j.brainres.2013.06.037. PMC 3839793. PMID 23835499.CS1 maint: multiple names: authors list (link)<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  • Liang CL, Marks GA (2014). "GABAA receptors are located in cholinergic terminals in the nucleus pontis oralis of the rat: implications for REM sleep control". Brain Res. 1543: 58–64. doi:10.1016/j.brainres.2013.10.019. PMID 24141149.<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  • Grace KP, Vanstone LE, Horner RL (2014). "Endogenous Cholinergic Input to the Pontine REM Sleep Generator Is Not Required for REM Sleep to Occur". J. Neurosci. 34 (43): 14198–209. doi:10.1523/JNEUROSCI.0274-14.2014. PMID 25339734.CS1 maint: multiple names: authors list (link)<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  • Carson III, Culley C., Kirby, Roger S., Goldstein, Irwin, editors, "Textbook of Erectile Dysfunction" Oxford, U.K.; Isis Medical Media, Ltd., 1999; Moreland, R.B. & Nehra, A.; Pathosphysiology of erectile dysfunction; a molecular basis, role of NPT in maintaining potency: pp. 105–15.

External links